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1 Dipartimento di Medicina, Chirurgia e Odontoiatria, Clinica Chirurgica Generale, Università degli Studi di Milano-Polo S. Paolo, Via A. Di Rudinì 8, I-20142 Milan, Italy
2 Laboratorio di Chimica Clinica e Microbiologia, Ospedale S. Paolo-Polo Universitario, Via A. Di Rudinì 8, I-20142 Milan, Italy
aAuthor for correspondence. Fax 39-02-8137613; e-mail giorgio.ghilardi{at}unimi.it.
Background: NO synthesized from L-arginine by the constitutive endothelial NO synthase (eNOS) plays a key role in the atherosclerotic process. We investigated whether common variants in the NOS3 gene (a T786C mutation in the 5' flanking region and the polymorphism on exon 7 that produced the Glu298Arg polymorphism in the protein) are associated with an increased risk of moderate to severe internal carotid artery (ICA) stenosis.
Methods: We studied 88 patients consecutively operated for ICA stenosis and 133 healthy controls. A T786C mutation in the 5' flanking region and the polymorphism in exon 7 that produces the Glu298Asp polymorphism in the protein were explored by PCR and fluorescent probe analysis.
Results: Genotype distribution was significantly different between patients and controls only for T786C, the CC genotype frequency being 26% and 13%, respectively [odds ratio (OR), 2.26; 95% confidence interval (CI), 1.14–4.46; P = 0.018]. Moreover, the CC genotype was significantly more frequent in a subgroup of patients with ulcerative plaques compared with patients with nonulcerative lesions (44% vs 17%; OR, 3.82; 95% CI, 1.79–8.14; P = 0.003). Multiple logistic regression analysis using the most frequent risk factors and the eNOS gene variant showed that the CC genotype is an independent risk factor for ICA stenosis (P = 0.023).
Conclusion: C allele homozygosity in position 786 of the eNOS promoter seems to be an independent risk factor for the development of moderate to severe ICA stenosis, especially ulcerative lesions.
The following articles in journals at HighWire Press have cited this article:
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  C. Napoli and L. J Ignarro Polymorphisms in endothelial nitric oxide synthase and carotid artery atherosclerosis J. Clin. Pathol., April 1, 2007; 60(4): 341 - 344. [Full Text] [PDF]
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 J. P. Casas, G. L. Cavalleri, L. E. Bautista, L. Smeeth, S. E. Humphries, and A. D. Hingorani Endothelial Nitric Oxide Synthase Gene Polymorphisms and Cardiovascular Disease: A HuGE Review Am. J. Epidemiol., November 15, 2006; 164(10): 921 - 935. [Abstract] [Full Text] [PDF]
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 C. Fatini, F. Sofi, A. M. Gori, E. Sticchi, R. Marcucci, M. Lenti, A. Casini, C. Surrenti, R. Abbate, and G. F. Gensini Endothelial Nitric Oxide Synthase -786T>C, but Not 894G>T and 4a4b, Polymorphism Influences Plasma Homocysteine Concentrations in Persons with Normal Vitamin Status Clin. Chem., July 1, 2005; 51(7): 1159 - 1164. [Abstract] [Full Text] [PDF]
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 M. Cattaruzza, T. J. Guzik, W. Slodowski, A. Pelvan, J. Becker, M. Halle, A. B. Buchwald, K. M. Channon, and M. Hecker Shear Stress Insensitivity of Endothelial Nitric Oxide Synthase Expression as a Genetic Risk Factor for Coronary Heart Disease Circ. Res., October 15, 2004; 95(8): 841 - 847. [Abstract] [Full Text] [PDF]
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 T. A. Manolio, E. Boerwinkle, C. J. O'Donnell, and A. F. Wilson Genetics of Ultrasonographic Carotid Atherosclerosis Arterioscler Thromb Vasc Biol, September 1, 2004; 24(9): 1567 - 1577. [Abstract] [Full Text] [PDF]
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M. G. Colombo, U. Paradossi, M. G. Andreassi, N. Botto, S. Manfredi, S. Masetti, A. Biagini, and A. Clerico Endothelial Nitric Oxide Synthase Gene Polymorphisms and Risk of Coronary Artery Disease Clin. Chem., March 1, 2003; 49(3): 389 - 395. [Abstract] [Full Text] [PDF]
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